Obstructive Sleep ApneaNCT05606991
The Effect of OSA on Brain Waste Clearance
A study testing CPAP Withdrawal in people with Obstructive Sleep Apnea and Dementia, run by Woolcock Institute of Medical Research at 1 site in Australia.
Trial summary
Recent ground-breaking research has shown that clearance of toxic neuro-metabolites from the brain including the proteins β-Amyloid (Aβ) and tau that form dementia causing plaques and tangles is markedly impaired when sleep is disturbed. Read more about this study
- Who is it for?
- Ages 35 to 65 yearsHealthy volunteers can take part
- Conditions the study is for
- Obstructive Sleep Apnea, Dementia, Cognitive Impairment
- What is being tested?
- CPAP Withdrawal
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 38 participants
- Where
- 1 siteAustralia
- Study dates
- 18 Jul 2023to Apr 2026
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 35 to 65 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Community dwelling adults aged 35-65 years.
- Polysomnography-confirmed severe OSA with apnea hypopnea index (AHI) ≥ 30/hour, with Non-Rapid Eye Movement (NREM) AHI ≥ 15/hour.
- Established CPAP use for treatment of OSA with compliance of > 3 months, with ≥ 5 hours use per night for > 5 nights per week.
- Willing to withdraw from CPAP use for 14 nights.
- Able to give informed verbal and written consent.
- Fluent in spoken, and comprehension of English.
Who cannot join
- Commercial drivers (e.g.: drivers of heavy vehicles, public passenger vehicles, or vehicles requiring dangerous goods driver license).
- History of severe cardiovascular disease (e.g.: stroke, myocardial infarction, atrial fibrillation).
- Presence of cognitive impairment and/or established diagnosis of dementia.
- Regular use of medications which affect sleep (e.g.: benzodiazepines, opioids, stimulants, sedating antihistamines).
- Regular 24-hour shift workers, presence of jetlag, or history of trans-meridian travel (crossing 2 or more time zones) in the past 2 weeks.
- Advice against withdrawal of CPAP treatment, as determined by the participant's treating physician or study physician.
Show all 14Show fewer
- Vulnerable to driving impairment without CPAP therapy/upon withdrawal of CPAP therapy, as assessed by: (a) positive response(s) to screening questions in the modified ASTN-Motor Vehicle Accident Questionnaire, reporting driving accidents and/or impairments prior to established CPAP therapy; AND/OR (b) the participant's treating physician.
- Prior history of severe COVID-19 infection involving significant neurological symptoms (e.g.: reduced level of consciousness, delirium, encephalopathy) - warranting hospitalization.
- Current COVID-19 infection and/or experience of ongoing symptoms/sequelae following a recent COVID-19 infection.
- Not up to date with the COVID-19 vaccination schedule - as per the current Australian Technical Advisory Group on Immunization (ATAGI) definition for individuals aged 16 years and over - at the time of writing this Protocol, defined as having:
- Received 2 primary doses of any Therapeutic Goods Administration (TGA)-approved or TGA-recognized COVID-19 vaccine at least 14 days apart (except for the Janssen COVID-19 vaccine, where only 1 primary dose is required); PLUS
- A booster dose of a TGA-approved COVID-19 vaccine (Pfizer, Moderna or AstraZeneca) at a recommended interval of 3-6 months after the receipt of 2nd primary dose; OR
- For severely immunocompromised individuals: received 3 primary doses of any TGA-approved or TGA-recognized COVID-19 vaccine, with dose 3 administered within 6 months of receiving dose 2.
- Other medical conditions deemed by study physicians to warrant exclusion.
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
Australia1 site
Woolcock Institute of Medical Research
Macquarie Park, New South Wales, 2113
About this study
Official title: The Impact of 2 Weeks CPAP Withdrawal on Brain Waste Clearance in Adults With Severe Obstructive Sleep Apnoea - A Randomised Controlled Crossover Trial
Recent ground-breaking research has shown that clearance of toxic neuro-metabolites from the brain including the proteins β-Amyloid (Aβ) and tau that form dementia causing plaques and tangles is markedly impaired when sleep is disturbed. This suggests that dementia risk may be increased in people with sleep disorders such as obstructive sleep apnea (OSA). Longitudinal studies have linked OSA with a 70-85% increased risk for mild cognitive impairment and dementia.
Despite this strong link, little is known about the OSA-specific mechanistic underpinnings. It is not fully understood as to how sleep disturbance in OSA inhibit brain glymphatic clearance. However, it is known that OSA inhibits slow wave sleep, profoundly activates sympathetic activity, and elevates blood pressure - particularly during sleep. These disturbances have, in turn, been shown to independently inhibit glymphatic function. Previous studies have attempted to sample human cerebrospinal fluid (CSF) involved in glymphatic clearance for dementia biomarkers during sleep. However, these studies were severely limited by the need for invasive CSF sampling. To address this problem, a set of newly available, highly sensitive blood based SIMOA assays will be used to study glymphatic function in people treated for severe OSA who undergo CPAP withdrawal. Furthermore, novel methods will be utilized to capture changes in slow wave sleep, blood pressure and brain blood flow together with sleep-wake changes in blood levels of excreted neuro-metabolites to define the pathophysiological mechanisms that inhibit brain cleaning in OSA.
Read the detailed description
Dementia is a neurodegenerative disease characterized by cognitive dysfunction affecting aspects of memory and learning. Although the mechanisms that underlie the pathophysiology of dementia are still unclear, in the past decade there has been a focus on the adverse impact of sleep disturbance on brain waste disposal via the glymphatic system. The glymphatic system is a recently discovered brain-wide perivascular passageway that transports toxic neuro-metabolites (e.g.: amyloid beta, or Aβ) out of the brain to the blood via the cerebrospinal fluid. Newer research has shown that the glymphatic system becomes particularly active during sleep, clearing metabolites twice as fast compared with wakefulness. Obstructive sleep apnea (OSA), a sleep disorder characterized by periods of intermittent hypoxia and sleep fragmentation due to obstructed breathing, has traditionally been causatively linked to the development of hypertension and cognitive dysfunction. Further to this, recent epidemiological studies have also linked OSA to an increased risk for both dementia and its prodromal state - mild cognitive impairment. There is emerging evidence to suggest that OSA might chronically impair glymphatic clearance of Aβ42 from the brain and facilitate the formation of Aβ plaques that characterize Alzheimer's Disease.
Recent ground-breaking research has shown that clearance of toxic neuro-metabolites from the brain including the proteins Aβ and tau that form dementia causing plaques and tangles is markedly impaired when sleep is disturbed. This suggests that dementia risk may be increased in people with sleep disorders such as OSA. Longitudinal studies have linked OSA with a 70-85% increased risk for mild cognitive impairment and dementia.
Despite this strong link, little is known about the OSA-specific mechanistic underpinnings. It is not fully understood as to how sleep disturbance in OSA inhibit brain glymphatic clearance. However, it is known that OSA inhibits slow wave sleep, profoundly activates sympathetic activity, and elevates blood pressure - particularly during sleep. These disturbances have, in turn, been shown to independently inhibit glymphatic function. Previous studies have attempted to sample human cerebrospinal fluid (CSF) involved in glymphatic clearance for dementia biomarkers during sleep. However, these studies were severely limited by the need for invasive CSF sampling. To address this problem, this proposed study will use a set of newly available, highly sensitive blood based SIMOA assays to study glymphatic function in people treated for severe OSA who undergo CPAP withdrawal. Furthermore, novel methods will be utilized to capture changes in slow wave sleep, blood pressure and brain blood flow together with sleep-wake changes in blood levels of excreted neuro-metabolites to define the pathophysiological mechanisms that inhibit brain cleaning in OSA.
- Conditions
- Obstructive Sleep Apnea, Dementia, Cognitive Impairment
- Being tested
- CPAP Withdrawal
- Keywords
- Obstructive sleep apnea, Brain waste clearance, Glymphatic system, Continuous positive airway pressure therapy, CPAP, Dementia, Cognitive impairment
- Medical subject headings
- Sleep Apnea, Obstructive, Dementia, Cognitive Dysfunction
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
CPAP WithdrawalOther
Complete withdrawal of continuous positive airway pressure (CPAP) therapy for a 2-week period.
| Study group | Role | What they receive |
|---|---|---|
| CPAP on | No intervention | Participants will continue with their usual continuous positive airway pressure (CPAP) therapy as advised by their treating physician. |
| CPAP off | Experimental | Participants will be weaned off their usual continuous positive airway pressure (CPAP) therapy and enter a 2-week period of non-treatment. Receives: Other: CPAP Withdrawal |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes in sleep-wake amplitudes (peak-trough) of blood levels of Aβ
Difference between the CPAP on and CPAP off conditions in sleep-wake amplitudes (peak-trough) of blood levels of Aβ (Aβ40/Aβ42 ratio), as measured by SIMOA blood neuro-metabolite assays.
Measured: Pre- and 2 weeks post-intervention
Secondary outcomes (7)
Changes in NREM slow wave parietal cortex activity
Differences between the CPAP on and CPAP off conditions in NREM slow wave parietal cortex activity as measured by high-density EEG (HD-EEG).
Measured: Pre- and 2 weeks post-intervention
Changes in brain tissue oxygenation during sleep
Differences between the CPAP on and CPAP off conditions in brain tissue oxygenation, as measured by oxygenated and deoxygenated hemoglobin using functional Near Infrared Spectroscopy (fNIRS).
Measured: Pre- and 2 weeks post-intervention
Changes in brain blood volume during sleep
Differences between the CPAP on and CPAP off conditions in brain blood volume during sleep, estimated by changes in total hemoglobin using functional Near Infrared Spectroscopy (fNIRS).
Measured: Pre- and 2 weeks post-intervention
Changes in sympathetic and parasympathetic activity during wake and sleep periods
Differences between the CPAP on and CPAP off conditions in sympathetic and parasympathetic activity during wake and sleep periods, as measured by heart rate variability (HRV) analysis of electrocardiogram (ECG) readings.
Measured: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of p-tau-217
Difference between the CPAP on and CPAP off conditions in sleep-wake amplitudes (peak-trough) of blood levels of p-tau-217, as measured by SIMOA blood neuro-metabolite assays.
Measured: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of glial fibrillary acidic protein (GFAP)
Difference between the CPAP on and CPAP off conditions in sleep-wake amplitudes (peak-trough) of blood levels of GFAP, as measured by SIMOA blood neuro-metabolite assays.
Measured: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of neurofilament light chain (NfL)
Difference between the CPAP on and CPAP off conditions in sleep-wake amplitudes (peak-trough) of blood levels of NfL, as measured by SIMOA blood neuro-metabolite assays.
Measured: Pre- and 2 weeks post-intervention
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Nov 2022
- Study start18 Jul 2023
- Primary completionApr 2026 (estimated)
- Study completionApr 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (9)Papers the sponsor has linked to this study.
- Other trials for Obstructive Sleep ApneaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Other
- Allocation
- Randomised
- Intervention model
- Crossover
- Model description
- Randomized controlled crossover trial
- Masking
- None (open label)
- Enrolment
- 38 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Woolcock Institute of Medical Research
- Sponsor type
- University, hospital or other
- Collaborators
- National Health and Medical Research Council, Australia
- Responsible party
- Sponsor
- Investigators
- Keith Wong, MBBS FRACP, Principal investigator, Woolcock Institute of Medical ResearchSvetlana Postnova, PhD, Principal investigator, University of SydneyMark Butlin, PhD, Principal investigator, Macquarie University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05606991
- Sponsor's protocol ID
- BrainOSA-0522
- Status last verified
- Jun 2025
- First submitted
- 12 Jul 2022
- Last updated
- 27 Jun 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Holth JK, Fritschi SK, Wang C, Pedersen NP, Cirrito JR, Mahan TE, Finn MB, Manis M, Geerling JC, Fuller PM, Lucey BP, Holtzman DM. The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans. Science. 2019 Feb 22;363(6429):880-884. doi: 10.1126/science.aav2546. Epub 2019 Jan 24.
PubMed 30679382Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM. Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle. Science. 2009 Nov 13;326(5955):1005-7. doi: 10.1126/science.1180962. Epub 2009 Sep 24.
PubMed 19779148Bubu OM, Andrade AG, Umasabor-Bubu OQ, Hogan MM, Turner AD, de Leon MJ, Ogedegbe G, Ayappa I, Jean-Louis G G, Jackson ML, Varga AW, Osorio RS. Obstructive sleep apnea, cognition and Alzheimer's disease: A systematic review integrating three decades of multidisciplinary research. Sleep Med Rev. 2020 Apr;50:101250. doi: 10.1016/j.smrv.2019.101250. Epub 2019 Dec 12.
PubMed 31881487Iliff JJ, Wang M, Liao Y, Plogg BA, Peng W, Gundersen GA, Benveniste H, Vates GE, Deane R, Goldman SA, Nagelhus EA, Nedergaard M. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta. Sci Transl Med. 2012 Aug 15;4(147):147ra111. doi: 10.1126/scitranslmed.3003748.
PubMed 22896675Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O'Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, Nedergaard M. Sleep drives metabolite clearance from the adult brain. Science. 2013 Oct 18;342(6156):373-7. doi: 10.1126/science.1241224.
PubMed 24136970Bucks RS, Olaithe M, Rosenzweig I, Morrell MJ. Reviewing the relationship between OSA and cognition: Where do we go from here? Respirology. 2017 Oct;22(7):1253-1261. doi: 10.1111/resp.13140. Epub 2017 Aug 4.
PubMed 28779504Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of Sleep-Disordered Breathing With Cognitive Function and Risk of Cognitive Impairment: A Systematic Review and Meta-analysis. JAMA Neurol. 2017 Oct 1;74(10):1237-1245. doi: 10.1001/jamaneurol.2017.2180.
PubMed 28846764Yaffe K, Laffan AM, Harrison SL, Redline S, Spira AP, Ensrud KE, Ancoli-Israel S, Stone KL. Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women. JAMA. 2011 Aug 10;306(6):613-9. doi: 10.1001/jama.2011.1115.
PubMed 21828324Ju YS, Zangrilli MA, Finn MB, Fagan AM, Holtzman DM. Obstructive sleep apnea treatment, slow wave activity, and amyloid-beta. Ann Neurol. 2019 Feb;85(2):291-295. doi: 10.1002/ana.25408. Epub 2019 Jan 17.
PubMed 30597615
Study at a glance
From the registry record, last updated by the sponsor on 27 Jun 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Impact of 2 Weeks CPAP Withdrawal on Brain Waste Clearance in Adults With Severe Obstructive Sleep Apnoea - A Randomised Controlled Crossover Trial
- ClinicalTrials.gov ID
- NCT05606991
- Acronym / sponsor ID
- BrainOSA-0522
- Conditions
- Obstructive Sleep Apnea, Dementia, Cognitive Impairment
- Keywords
- Obstructive sleep apnea, Brain waste clearance, Glymphatic system, Continuous positive airway pressure therapy, CPAP, Dementia, Cognitive impairment
- Study type
- Interventional
- Recruitment status
- Enrolling by invitation
- Enrolment
- 38 participants (estimated)
- Lead sponsor
- Woolcock Institute of Medical ResearchUniversity, hospital or other
- Collaborators
- National Health and Medical Research Council, Australia
- Study start
- 18 Jul 2023 (actual)
- Primary completion
- Apr 2026 (estimated)
- Study completion
- Apr 2026 (estimated)
- First posted
- 7 Nov 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Recent ground-breaking research has shown that clearance of toxic neuro-metabolites from the brain including the proteins β-Amyloid (Aβ) and tau that form dementia causing plaques and tangles is markedly impaired when sleep is disturbed. This suggests that dementia risk may be increased in people with sleep disorders such as obstructive sleep apnea (OSA). Longitudinal studies have linked OSA with a 70-85% increased risk for mild cognitive impairment and dementia.
Despite this strong link, little is known about the OSA-specific mechanistic underpinnings. It is not fully understood as to how sleep disturbance in OSA inhibit brain glymphatic clearance. However, it is known that OSA inhibits slow wave sleep, profoundly activates sympathetic activity, and elevates blood pressure - particularly during sleep. These disturbances have, in turn, been shown to independently inhibit glymphatic function. Previous studies have attempted to sample human cerebrospinal fluid (CSF) involved in glymphatic clearance for dementia biomarkers during sleep. However, these studies were severely limited by the need for invasive CSF sampling. To address this problem, a set of newly available, highly sensitive blood based SIMOA assays will be used to study glymphatic function in people treated for severe OSA who undergo CPAP withdrawal. Furthermore, novel methods will be utilized to capture changes in slow wave sleep, blood pressure and brain blood flow together with sleep-wake changes in blood levels of excreted neuro-metabolites to define the pathophysiological mechanisms that inhibit brain cleaning in OSA.
Detailed description
Dementia is a neurodegenerative disease characterized by cognitive dysfunction affecting aspects of memory and learning. Although the mechanisms that underlie the pathophysiology of dementia are still unclear, in the past decade there has been a focus on the adverse impact of sleep disturbance on brain waste disposal via the glymphatic system. The glymphatic system is a recently discovered brain-wide perivascular passageway that transports toxic neuro-metabolites (e.g.: amyloid beta, or Aβ) out of the brain to the blood via the cerebrospinal fluid. Newer research has shown that the glymphatic system becomes particularly active during sleep, clearing metabolites twice as fast compared with wakefulness. Obstructive sleep apnea (OSA), a sleep disorder characterized by periods of intermittent hypoxia and sleep fragmentation due to obstructed breathing, has traditionally been causatively linked to the development of hypertension and cognitive dysfunction. Further to this, recent epidemiological studies have also linked OSA to an increased risk for both dementia and its prodromal state - mild cognitive impairment. There is emerging evidence to suggest that OSA might chronically impair glymphatic clearance of Aβ42 from the brain and facilitate the formation of Aβ plaques that characterize Alzheimer's Disease.
Recent ground-breaking research has shown that clearance of toxic neuro-metabolites from the brain including the proteins Aβ and tau that form dementia causing plaques and tangles is markedly impaired when sleep is disturbed. This suggests that dementia risk may be increased in people with sleep disorders such as OSA. Longitudinal studies have linked OSA with a 70-85% increased risk for mild cognitive impairment and dementia.
Despite this strong link, little is known about the OSA-specific mechanistic underpinnings. It is not fully understood as to how sleep disturbance in OSA inhibit brain glymphatic clearance. However, it is known that OSA inhibits slow wave sleep, profoundly activates sympathetic activity, and elevates blood pressure - particularly during sleep. These disturbances have, in turn, been shown to independently inhibit glymphatic function. Previous studies have attempted to sample human cerebrospinal fluid (CSF) involved in glymphatic clearance for dementia biomarkers during sleep. However, these studies were severely limited by the need for invasive CSF sampling. To address this problem, this proposed study will use a set of newly available, highly sensitive blood based SIMOA assays to study glymphatic function in people treated for severe OSA who undergo CPAP withdrawal. Furthermore, novel methods will be utilized to capture changes in slow wave sleep, blood pressure and brain blood flow together with sleep-wake changes in blood levels of excreted neuro-metabolites to define the pathophysiological mechanisms that inhibit brain cleaning in OSA.
Study design
- Primary purpose
- Other
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- Randomized controlled crossover trial
| Arm | Type | Receives |
|---|---|---|
| CPAP on | No intervention | –Participants will continue with their usual continuous positive airway pressure (CPAP) therapy as advised by their treating physician. |
| CPAP off | Experimental | Other: CPAP WithdrawalParticipants will be weaned off their usual continuous positive airway pressure (CPAP) therapy and enter a 2-week period of non-treatment. |
Who may qualify
- Ages
- 35 to 65 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (6 listed)
- Community dwelling adults aged 35-65 years.
- Polysomnography-confirmed severe OSA with apnea hypopnea index (AHI) ≥ 30/hour, with Non-Rapid Eye Movement (NREM) AHI ≥ 15/hour.
- Established CPAP use for treatment of OSA with compliance of > 3 months, with ≥ 5 hours use per night for > 5 nights per week.
- Willing to withdraw from CPAP use for 14 nights.
- Able to give informed verbal and written consent.
Key exclusion criteria (14 listed)
- Commercial drivers (e.g.: drivers of heavy vehicles, public passenger vehicles, or vehicles requiring dangerous goods driver license).
- History of severe cardiovascular disease (e.g.: stroke, myocardial infarction, atrial fibrillation).
- Presence of cognitive impairment and/or established diagnosis of dementia.
- Regular use of medications which affect sleep (e.g.: benzodiazepines, opioids, stimulants, sedating antihistamines).
- Regular 24-hour shift workers, presence of jetlag, or history of trans-meridian travel (crossing 2 or more time zones) in the past 2 weeks.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| CPAP WithdrawalComplete withdrawal of continuous positive airway pressure (CPAP) therapy for a 2-week period. | Other | CPAP off |
Primary outcome
Changes in sleep-wake amplitudes (peak-trough) of blood levels of Aβ
Time frame: Pre- and 2 weeks post-intervention
Difference between the CPAP on and CPAP off conditions in sleep-wake amplitudes (peak-trough) of blood levels of Aβ (Aβ40/Aβ42 ratio), as measured by SIMOA blood neuro-metabolite assays.
7 secondary outcomes
Changes in NREM slow wave parietal cortex activity
Time frame: Pre- and 2 weeks post-intervention
Changes in brain tissue oxygenation during sleep
Time frame: Pre- and 2 weeks post-intervention
Changes in brain blood volume during sleep
Time frame: Pre- and 2 weeks post-intervention
Changes in sympathetic and parasympathetic activity during wake and sleep periods
Time frame: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of p-tau-217
Time frame: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of glial fibrillary acidic protein (GFAP)
Time frame: Pre- and 2 weeks post-intervention
Changes in sleep-wake amplitudes (peak-trough) of blood levels of neurofilament light chain (NfL)
Time frame: Pre- and 2 weeks post-intervention
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 27 Jun 2025.
- Background: PubMed 30679382Holth JK, Fritschi SK, Wang C, Pedersen NP, Cirrito JR, Mahan TE, Finn MB, Manis M, Geerling JC, Fuller PM, Lucey BP, Holtzman DM. The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans. Science. 2019 Feb 22;363(6429):880-884. doi: 10.1126/science.aav2546. Epub 2019 Jan 24.
- Background: PubMed 19779148Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM. Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle. Science. 2009 Nov 13;326(5955):1005-7. doi: 10.1126/science.1180962. Epub 2009 Sep 24.
- Background: PubMed 31881487Bubu OM, Andrade AG, Umasabor-Bubu OQ, Hogan MM, Turner AD, de Leon MJ, Ogedegbe G, Ayappa I, Jean-Louis G G, Jackson ML, Varga AW, Osorio RS. Obstructive sleep apnea, cognition and Alzheimer's disease: A systematic review integrating three decades of multidisciplinary research. Sleep Med Rev. 2020 Apr;50:101250. doi: 10.1016/j.smrv.2019.101250. Epub 2019 Dec 12.
- Background: PubMed 22896675Iliff JJ, Wang M, Liao Y, Plogg BA, Peng W, Gundersen GA, Benveniste H, Vates GE, Deane R, Goldman SA, Nagelhus EA, Nedergaard M. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta. Sci Transl Med. 2012 Aug 15;4(147):147ra111. doi: 10.1126/scitranslmed.3003748.
- Background: PubMed 24136970Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O'Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, Nedergaard M. Sleep drives metabolite clearance from the adult brain. Science. 2013 Oct 18;342(6156):373-7. doi: 10.1126/science.1241224.
- Background: PubMed 28779504Bucks RS, Olaithe M, Rosenzweig I, Morrell MJ. Reviewing the relationship between OSA and cognition: Where do we go from here? Respirology. 2017 Oct;22(7):1253-1261. doi: 10.1111/resp.13140. Epub 2017 Aug 4.
- Background: PubMed 28846764Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of Sleep-Disordered Breathing With Cognitive Function and Risk of Cognitive Impairment: A Systematic Review and Meta-analysis. JAMA Neurol. 2017 Oct 1;74(10):1237-1245. doi: 10.1001/jamaneurol.2017.2180.
- Background: PubMed 21828324Yaffe K, Laffan AM, Harrison SL, Redline S, Spira AP, Ensrud KE, Ancoli-Israel S, Stone KL. Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women. JAMA. 2011 Aug 10;306(6):613-9. doi: 10.1001/jama.2011.1115.
- Background: PubMed 30597615Ju YS, Zangrilli MA, Finn MB, Fagan AM, Holtzman DM. Obstructive sleep apnea treatment, slow wave activity, and amyloid-beta. Ann Neurol. 2019 Feb;85(2):291-295. doi: 10.1002/ana.25408. Epub 2019 Jan 17.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Keith Wong, MBBS FRACP principal investigator
Woolcock Institute of Medical Research
Svetlana Postnova, PhD principal investigator
University of Sydney
Mark Butlin, PhD principal investigator
Macquarie University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing CPAP Withdrawal in people with Obstructive Sleep Apnea and Dementia, run by Woolcock Institute of Medical Research at 1 site in Australia.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 14 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: enrolling by invitation, as of the sponsor's last update on 27 Jun 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Australia. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Changes in sleep-wake amplitudes (peak-trough) of blood levels of Aβ (time frame: Pre- and 2 weeks post-intervention). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05606991, which also lists 9 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 27 Jun 2025.